Category Filter
- Advanced Imaging
- Autism Spectrum Mandate
- Behavioral Health
- Blue Advantage Policies
- Chronic Condition Management
- Genetic Testing
- HelpScript Program
- Hemophilia Drugs
- Medical Policies
- Pre-Service Review (Predetermination/Precertification)
- Provider-Administered Drug Policies
- Radiation Therapy
- Self-Administered Drug Policies
- Transgender Services
Asset Publisher
Interleukin-5 (IL-5) Inhibitors Prior Authorization with Quantity Limit Program Summary
Policy Number: PH-1115
This program applies to Blue Partner, Commercial, GenPlus, NetResults A series, SourceRx and Health Insurance Marketplace formularies.
POLICY REVIEW CYCLE
Effective Date |
Date of Origin |
07-01-2024 |
|
FDA LABELED INDICATIONS AND DOSAGE
Agent(s) |
FDA Indication(s) |
Notes |
Ref# |
Fasenra® (benralizumab) Injection for subcutaneous use |
Add-on maintenance treatment of patients with severe asthma aged 12 years and older, and with an eosinophilic phenotype Limitations of use:
|
|
2 |
Nucala® (mepolizumab) Injection for subcutaneous use |
Add-on maintenance treatment of patients aged 6 years and older with severe asthma and with an eosinophilic phenotype Treatment of adult patients with eosinophilic granulomatosis with polyangiitis (EGPA) Treatment of adult and pediatric patients aged 12 years and older with hypereosinophilic syndrome (HES) for greater than or equal to 6 months without an identifiable non-hematologic secondary cause Add-on maintenance treatment of chronic rhinosinusitis with nasal polyps (CRSwNP) in adult patients 18 years of age and older with inadequate response to nasal corticosteroids Limitation of use:
|
|
1 |
See package insert for FDA prescribing information: https://dailymed.nlm.nih.gov/dailymed/index.cfm
CLINICAL RATIONALE
Asthma |
Asthma is a chronic inflammatory disorder of the airways.(3,5) It is characterized by variable and recurring clinical symptoms, airflow obstruction, bronchial hyperresponsiveness, and underlying inflammation.(3) Symptoms of asthma include wheezing, coughing, recurrent difficulty breathing, shortness of breath, and chest tightness. Generally, these symptoms will occur or worsen with exposure to allergens and irritants, infections, exercise, changes in weather, stress, or menstrual cycles. Guidelines recommend the use of detailed medical history, physical examination, and spirometry to make a diagnosis of asthma.(3,5) The Global Initiative for Asthma (GINA) guidelines recommend a stepwise approach for managing asthma. Long-term goals for asthma management are to achieve good control of symptoms, maintain normal activity level, and to minimize the future risk of exacerbations, fixed airflow limitation, and side-effects.(5) IgE is the antibody responsible for activation of allergic reactions and is important to the pathogenesis of allergic asthma and the development and persistence of inflammation. GINA guidelines define moderate asthma as that which is well controlled with Step 3 or Step 4 treatment (e.g., low- or medium-dose inhaled corticosteroids [ICS] in combination with a long-acting beta agonist [LABA] in either treatment track). Severe asthma is defined as asthma that remains uncontrolled despite optimized treatment with high-dose ICS-LABA, or that requires high-dose ICS-LABA to prevent it from becoming uncontrolled. Severe asthma must be distinguished from asthma that is difficult to treat due to inadequate or inappropriate treatment, or persistent problems with adherence or comorbidities such as chronic rhinosinusitis or obesity, as they need very different treatment compared with if asthma is relatively refractory to high-dose ICS-LABA or even oral corticosteroids (OCS). Early initiation of low dose ICS in patients with asthma has led to greater improvement in lung function than initiation of ICS after symptoms have been present for more than 2 to 4 years. The 2023 GINA guidelines recommend every adult and adolescent with asthma should receive ICS-containing controller medication to reduce the risk of serious exacerbation, even in patients with infrequent symptoms.(5) 2023 GINA STEP recommendations for adults and adolescents (12 years of age and over) are intended to reduce the risk of serious exacerbations and are broken into two tracks based on reliever therapy. Track 1 is the preferred approach recommended by GINA, because using low dose ICS-formoterol as reliever reduces the risk of exacerbations compared with regimens with short-acting β2-agonist (SABA) as reliever, and is a simpler regimen. Note ICS-formoterol should not be used as the reliever by patients taking any other (non-formoterol) ICS-LABA or ICS-LAMA:(5)
Track 2 is an alternative approach if Track 1 is not possible or is not preferred by a patient with no exacerbations on their current therapy. Before considering a regimen with SABA reliever, the clinician should consider whether the patient is likely to be adherent with their controller therapy; if not, they will be exposed to the higher risk of exacerbations with SABA-only treatment:(5)
2023 GINA STEP recommendations for children (6 to 11 years of age) are intended to reduce the risk of serious exacerbations:(5)
Severe Asthma Phenotype and Eosinophilic Asthma Subphenotype Roughly 3% to 10% of adults with asthma have severe asthma as defined by the GINA 2023 guidelines.(5) The European Respiratory Society (ERS)/American Thoracic Society (ATS) guidelines (2014; updated 2020) and the National Asthma Education and Prevention Program Coordinating Committee Expert Panel Working Group mirror the GINA definition of severe asthma, and defined uncontrolled asthma for adult and pediatric patients 5 years of age and over:(3,19)
A specialist, preferably in a multidisciplinary severe asthma clinic (if available) performs further assessment, which includes the patient’s inflammatory phenotype (i.e., Type 2 or non-Type 2).(5) Type 2 inflammation is characterized by the presence of cytokines such as interleukin (IL)-4, IL-5, and IL-13, which are often produced by the adaptive immune system on recognition of allergens. It is also characterized by eosinophilia or increased fraction of exhaled nitric oxide (FeNO) and may be accompanied by atopy. In many patients with asthma, Type 2 inflammation rapidly improves when ICS are taken regularly and correctly; this is classified as mild or moderate asthma. In severe asthma, Type 2 inflammation may be relatively refractory to high dose ICS. Type 2 inflammation is considered refractory if any of the following are found while the patient is taking high dose ICS or daily OCS:(5)
Biologic agents should be considered as add-on therapy for patients with refractory Type 2 inflammation with exacerbations or poor symptom control despite taking at least high dose ICS/LABA, and who have allergic or eosinophilic biomarkers or need maintenance OCS.(5) 2023 GINA recommends the biologics below based on patient eligibility factors:
Patient response should be evaluated 4 months after initiating therapy and follow up should occur every 3 to 6 months thereafter. 2023 GINA recommends the following step-down therapy process in patients responding well to targeted biologic therapy:(5)
|
||||||||||||||||||||
Eosinophilic Granulomatosis with Polyangiitis (EGPA) |
Eosinophilic granulomatosis with polyangiitis (EGPA), formally known as Churg-Strauss Syndrome, is a rare small-vessel vasculitis that occurs in patients with asthma and eosinophilia and is histologically characterized by tissue eosinophilia, necrotizing vasculitis and eosinophil-rich granulomatous inflammation. EGPA is an anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis, characterized by asthma, eosinophilia and granulomatous or vasculitic involvement of several organs. Current practice relies on recommendations and guidelines addressing the management of ANCA-associated vasculitis and not specifically developed for EGPA.(20) The main clinical features of EGPA are late-onset allergic rhinitis and asthma, increased blood eosinophil count, and vasculitis manifestations, some of which can be life threatening. Once EGPA is suspected based on clinical findings of asthma with eosinophilia, asthma with systemic manifestations, or even eosinophilia with extrapulmonary disease, a biopsy demonstrating small or medium sized vessel vasculitis strongly supports the diagnosis of EGPA. Skin, nerve, and muscle are among the most common biopsied tissues, but endomyocardial, renal, and gastrointestinal biopsies may also be useful. Antineutrophil cytoplasm antibody (ANCA) testing is also recommended. ANCA positivity is highly suggestive of EGPA, but ANCA negative results do not rule out its diagnosis.(6) The clinical phenotype of EGPA is quite heterogeneous and the diagnosis is not always straightforward. Anti-neutrophil cytoplasmic antibodies (ANCA), usually against myeloperoxidase (MPO), are detectable in approximately 40% of the cases and are associated with a different frequency of clinical manifestations: features of vasculitis, particularly glomerulonephritis, peripheral neuropathy and purpura, occur more often in ANCA-positive patients, whereas the so-called eosinophilic features such as cardiac involvement and gastroenteritis are more frequent in ANCA-negative patients.(20) There are two types of classifications used for the diagnosis of EGPA. The first and most commonly used classification is by the American College of Rheumatology (ACR). ACR has established six criteria for the classification of EGPA in a patient with documented vasculitis. The presence of four or more of these criteria can establish a diagnosis of EGPA:(7)
The Lanham criteria is also used for the diagnosis of EGPA. The Lanham criteria requires the patient to have all three of the following: asthma, peak peripheral blood eosinophilia in excess of 1500 cells/microliter, and systemic vasculitis involving two or more extra-pulmonary organs.(7,8) The American College of Rheumatology/European Alliance of Associations for Rheumatology developed classification criteria for EGPA broken into clinical criteria as well as laboratory and biopsy criteria. Considerations when applying these criteria(20)
The Five-Factor Score (FFS) predicts the risk of mortality in patients with an established diagnosis of EGPA, as well as polyarteritis nodosa microscopic polyangiitis or GPA. It includes five factors associated with shortened overall survival, namely, renal insufficiency (serum creatinine > 1.58 mg/dl), proteinuria > 1 g per day, cardiomyopathy, gastrointestinal involvement and central nervous system (CNS) involvement. The FFS considers clinical manifestations only at the time of diagnosis, the appearance of new manifestations during follow-up should also be taken into account when choosing remission-induction regimens for disease flares. New-onset active EGPA is considered severe if FFS is greater than or equal to 1 or there is presence of peripheral neuropathy, alveolar hemorrhage or other organ-or life-threatening manifestations. For relapsing EGPA severe disease consists of severe systemic relapse and non-severe is respiratory relapse alone or non-severe systemic relapse.(20) For remission induction in patients with new-onset, active EGPA, glucocorticoids should be administered as initial therapy. In patients with severe disease cyclophosphamide or rituximab and/or disease modifying anti-rheumatic drugs (DMARDs) should be added to glucocorticoid therapy. Remission maintenance for non-severe disease guidelines recommend glucocorticoids plus mepolizumab. Remission maintenance for severe disease guidelines recommend glucocorticoids plus rituximab and/or mepolizumab and or DMARDs. Although the evidence supporting the use of traditional immunosuppressants for remission maintenance in non-severe EGPAS is scarce, these agents are often used in routine clinical practice.(20) Treatment for relapsing EGPA in non-severe disease glucocorticoids alone or glucocorticoids plus mepolizumab along with optimization of inhaled therapies. Treatment of relapsing severe disease high-dose oral glucocorticoids plus cyclophosphamide or rituximab is recommended.(20) Refractory EGPA is defined as unchanged or increased disease activity after 4 weeks of appropriate remission-induction therapy. The persistence or worsening of systemic manifestations should be distinguished from that of respiratory manifestations. Mepolizumab in combination with glucocorticoids is recommended to induce remission in patients with relapsing-refractory EGPA without organ-or life-threatening manifestations. Mepolizumab can also be used for remission maintenance, particularly in patients requiring a daily prednisone greater than or equal to 7.5 mg for the control of their respiratory manifestations.(20) |
||||||||||||||||||||
Hypereosinophilic Syndrome (HES) |
The eosinophilias encompass a broad range of non‐hematologic (secondary or reactive) and hematologic (primary or clonal) disorders with potential for end‐organ damage. Hypereosinophilia (HE) has generally been defined as peripheral blood eosinophil count greater than 1500 cells/microliter, OR pathologic confirmation of tissue HE by at least one of the following: percentage of eosinophils in bone marrow section exceeds 20% of all nucleated cells, marked deposition of eosinophil granule proteins is found, or tissue infiltration by eosinophils is extensive in the opinion of the pathologist.(12) To establish a diagnosis of HES, all three of the following criteria must be met:(11,12,13)
Although the clinical manifestations can be similar irrespective of the cause of the eosinophilia, the choice of the initial therapeutic agent(s) for a given patient depends mainly on whether the patient has clinical features consistent with a myeloid disorder. Patients with myeloid variants of HES (e.g., PDGFRA-positive HES) often have an aggressive course with disabling complications and high mortality in the absence of treatment, and are treated initially with imatinib; those with other types of HES are treated with an initial trial of glucocorticoids.(11,12,13,14) Oral corticosteroids have been used for decades in the treatment of HES and, with the exception of imatinib for PDGFRA-associated HES as noted above, remain the first-line treatment for most patients. Hydroxyurea is a typical second-line agent, whether used as monotherapy or in conjunction with corticosteroids. Additional immunomodulatory and cytotoxic agent options include interferon-α, azathioprine, cyclosporine, methotrexate, and tacrolimus.(12,13,14) Despite the wide variety of commercially available immunomodulatory and cytotoxic agents, a significant proportion of patients with HES are treatment-refractory or experience treatment-related toxicity. Monoclonal anti–IL-5 antibody therapy for HES has a number of unique advantages related to the specificity of IL-5 for the eosinophil lineage.(12,13,14) |
||||||||||||||||||||
Chronic Rhinosinusitis with Nasal Polyposis |
Chronic rhinosinusitis with nasal polyposis (CRSwNP) is an inflammatory condition affecting the paranasal sinuses. The International Consensus Statement on allergy and rhinology: Rhinosinusitis indicates that the diagnostic criteria for chronic rhinosinusitis (CRS) consist of ALL the following:(18)
Sinus computed tomography (CT) and/or nasal endoscopy are needed to determine the presence of sinonasal inflammation and nasal polyps. The exact cause of CRSwNP is unknown, but biopsies of nasal polyps have shown elevated levels of eosinophils.(15) Intranasal corticosteroids (INCS) are recommended in the guidelines for CRSwNP. There are several formulations of INCS and it is recommended that clinicians must help each patient arrive at a management decision consistent with that patient's values and preferences as no formulation is recommended over another. For patients using INCS for at least 4 weeks and who continue to have high disease burden, biologics are preferred over other medical treatment choices. Biologics vary in their magnitude of benefits and harms and certainty of evidence across outcomes. For outcomes most important to patient care, dupilumab and omalizumab are the most beneficial, followed by mepolizumab. Other management options for CRSwNP that patients and their caregivers could consider include saline rinse, surgery, antibiotics, and for people with aspirin (non-steroidal anti-inflammatory)-exacerbated respiratory disease consider using aspirin therapy after desensitization.(16) |
||||||||||||||||||||
Efficacy |
Asthma Fasenra Benralizumab was approved through 3 confirmatory clinical trials. Trial 1 and Trial 2 were exacerbation trials in patients 12 years of age and older. All subjects continued their background asthma therapy throughout the duration of the trials. The primary endpoint was the rate of asthma exacerbations in patients who were taking high-dose ICS and LABA. Asthma exacerbation was defined as a worsening of asthma requiring use of oral/systemic corticosteroids for at least 3 days, and/or emergency department visits requiring use of oral/systemic corticosteroids and/or hospitalization. For patients on maintenance oral corticosteroids, an asthma exacerbation requiring oral corticosteroids was defined as a temporary increase in stable oral/systemic corticosteroids for at least 3 days or a single depo-injectable dose of corticosteroids. In Trial 1, 35% of patients receiving benralizumab experienced an asthma exacerbation compared to 51% on placebo. In Trial 2, 40% of patients receiving benralizumab experienced an asthma exacerbation compared to 51% on placebo.(2) Trial 3 was a randomized OCS reduction trial in asthma patients. Patients were required to be treated with daily OCS (7.5 to 40 mg per day) in addition to regular use of high-dose ICS and LABA with or without additional controller(s). The trial included an 8-week run-in period during which the OCS was titrated to the minimum effective dose without losing asthma control. For the purposes of the OCS dose titration, asthma control was assessed by the investigator based on a patient’s FEV1, peak expiratory flow, nighttime awakenings, short-acting bronchodilator rescue medication use or any other symptoms that would require an increase in OCS dose. Fasenra achieved greater reductions in daily maintenance OCS dose while maintaining asthma control compared to placebo (median reduction of 75% for Fasenra vs 25% for placebo).(2) Nucala The efficacy of mepolizumab for the treatment of severe eosinophilic asthma was established in three double-blind, randomized, placebo-controlled trials: A dose-ranging and exacerbation reduction trial (trial 1) and two confirmatory trials (trial 2 and 3). All subjects continued their background asthma therapy throughout the duration of the trials. Trial 1 enrolled subjects with uncontrolled asthma despite use of high dose inhaled corticosteroids (ICS) plus additional controller(s), with or without OCS. Trial 2 was a placebo- and active-controlled trial in subjects with asthma not adequately controlled on high-dose inhaled corticosteroids plus additional controller(s) with or without OCS. The primary end point for trial 1 and 2 was frequency of asthma exacerbations. Compared to placebo, subjects receiving mepolizumab experienced significantly fewer exacerbations and had a longer time to first exacerbation.(1) Trial 3 was an OCS-reduction study in asthma patients who required daily OCS in addition to regular controller medications. The primary end point was percent reduction of OCS dose during weeks 20 to 24 without loss of asthma control. The baseline mean oral corticosteroid use was similar between the Nucala and placebo group. Overall, mepolizumab achieved greater reduction in oral corticosteroid use while maintaining asthma control when compared to placebo. However, the difference between the mepolizumab and placebo groups was not statistically significant.(1)
EGPA Nucala A total of 136 subjects with EGPA were evaluated in a randomized, placebo-controlled, multicenter, 52-week trial. Subjects enrolled had a diagnosis of EGPA for at least 6 months prior to enrollment with a history of relapsing or refractory disease and were on a stable dosage of oral prednisolone or prednisone of greater than or equal to 7.5 mg/day (but not greater than 50 mg/day) for at least 4 weeks prior to enrollment. Subjects received 300 mg of mepolizumab or placebo administered subcutaneously once every 4 weeks while continuing their stable OCS therapy. Starting at Week 4, OCS was tapered during the treatment period at the discretion of the investigator. The co-primary endpoints were the total accrued duration of remission over the 52-week treatment period, defined as Birmingham Vasculitis Activity Score (BVAS) = 0 (no active vasculitis) plus prednisolone or prednisone dose less than or equal to 4 mg/day, and the proportion of subjects in remission at both Week 36 and Week 48 of treatment. The BVAS is a clinician-completed tool to assess clinically active vasculitis that would likely require treatment, after exclusion of other causes.(1) A significantly higher proportion of subjects receiving mepolizumab achieved remission at both Week 36 and Week 48 compared with placebo. In addition, significantly more subjects receiving mepolizumab achieved remission within the first 24 weeks and remained in remission for the remainder of the 52-week study treatment period compared with placebo (19% for mepolizumab versus 1% for placebo; OR 19.7; 95% CI: 2.3, 167.9).(1) The time to first relapse (defined as worsening related to vasculitis, asthma, or sino-nasal symptoms requiring an increase in dose of corticosteroids or immunosuppressive therapy or hospitalization) was significantly longer for subjects receiving mepolizumab compared with placebo with a hazard ratio of 0.32 (95% CI: 0.21, 0.5). Additionally, subjects receiving mepolizumab had a reduction in rate of relapse compared with subjects receiving placebo (rate ratio 0.50; 95% CI: 0.36, 0.70 for mepolizumab compared with placebo). The incidence and number of relapse types (vasculitis, asthma, sino-nasal) were numerically lower with mepolizumab compared with placebo.(1) Subjects receiving mepolizumab had a significantly greater reduction in average daily OCS dose compared with subjects receiving placebo during Weeks 48 to 52.(1)
HES Nucala A total of 108 adult and adolescent patients aged 12 years and older with HES for at least 6 months were evaluated in a randomized, double-blind, placebo-controlled, multicenter, 32-week trial (NCT #02836496). Patients with non-hematologic secondary HES (e.g., drug hypersensitivity, parasitic helminth infection, HIV infection, non-hematologic malignancy) or FIP1L1-PDGFRα kinase-positive HES were excluded from the trial. Patients received 300 mg of Nucala or placebo subcutaneously once every 4 weeks while continuing their stable HES therapy. Patients entering the trial had experienced at least 2 HES flares within the past 12 months and a blood eosinophil count of 1,000 cells/microliter or higher during screening. Historical HES flares for the trial entry criteria were defined as HES-related worsening of clinical symptoms or blood eosinophil counts requiring an escalation in therapy. Patients must have been on stable background HES therapy for a minimum of 4 weeks prior to randomization; existing HES therapy was maintained throughout the treatment period unless there was symptom worsening that required a dose increase. HES therapy could include chronic or episodic oral corticosteroids (OCS), immunosuppressive, and/or cytotoxic therapy.(1,10) The efficacy of Nucala in HES was established based upon the proportion of patients who experienced a HES flare during the 32-week treatment period. A HES flare was defined as worsening of clinical signs and symptoms of HES or increasing eosinophils (on at least 2 occasions), resulting in the need to increase OCS or increase/add cytotoxic or immunosuppressive HES therapy. Over the 32-week treatment period, the incidence of HES flare over the treatment period was 56% for the placebo group and 28% for the group treated with Nucala (50% reduction).(1,10)
CRSwNP Nucala A randomized, double-blind, multicenter, placebo-controlled 52-week trial (NCT03085797) evaluated Nucala in patients with CRSwNP. The trial inclusion requirements included adult patients on background intranasal corticosteroids (INCS), with recurrent and symptomatic CRSwNP despite at least 1 surgery for the removal of nasal polyps within the previous 10 years. A total of 407 subjects were randomized to receive either 100 mg Nucala (N=206) or placebo (N=201) every 4 weeks for 52 weeks (13 doses). All study participants received mometasone furoate 400 mcg (intolerant participants received 200mcg) daily along with Nucala or placebo. Participants were not required to have sinus CT scans, but were required to have endoscopic confirmation of diagnosis.(1) The co-primary efficacy endpoints were change from baseline to Week 52 in total endoscopic nasal polyps score (NPS; 0-8 scale) as graded by independent blinded assessors and change from baseline in nasal visual analog scale (VAS; 0-10 scale) during weeks 49 to 52.(1) Statistically significant efficacy was observed regarding improvement (decrease) in bilateral endoscopic NPS score at week 52, and nasal obstruction VAS score from weeks 49 to 52. Total endoscopic NPS significantly improved at week 52 from baseline with mepolizumab versus placebo (adjusted difference in medians -0.73, 95% CI -1.11 to -0.34; p less than 0.001) and nasal obstruction VAS score during weeks 49–52 also significantly improved (-3.14, -4.09 to -2.18; p less than 0.001).(1) Treatment with Nucala resulted in significant reduction of systemic corticosteroid use and need for sinonasal surgery versus placebo. The proportion of subjects who required surgery was reduced by 57% (HR of 0.43; 95% CI: 0.25, 0.76). Treatment with Nucala also significantly reduced the need for systemic steroids for nasal polyps versus placebo.(1) |
||||||||||||||||||||
Safety |
Benralizumab and mepolizumab have not been studied for use in combination with Xolair (omalizumab). |
REFERENCES
Number |
Reference |
1 |
Nucala prescribing information. GlaxoSmithKline LLC. March 2023. |
2 |
Fasenra prescribing information. AstraZeneca Pharmaceuticals LP. February 2021. |
3 |
International European Respiratory Society (ERS)/American Thoracic Society (ATS) Guidelines on Management of Severe Asthma. Eur Resp J. 2020;55:1900588. Available at https://erj.ersjournals.com/content/55/1/1900588. |
4 |
Reference no longer used |
5 |
Global Initiative for Asthma (GINA). Global Strategy for Asthma Management and Prevention. 2023. Available at www.ginasthma.org. |
6 |
Groh M, Pagnoux C, Baldini C, et al. Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss) (EGPA) Consensus Task Force Recommendations for Evaluation and Management. Eur J Intern Med. 2015;26(7):545-553. |
7 |
Masi AT, Hunder GG, Lie JT, et al. The American College of Rheumatology 1990 Criteria for the Classification of Churg-Strauss Syndrome (Allergic Granulomatosis and Angiitis). Arthritis Rheum. 1990;33(8):1094-1100. |
8 |
Lanham JG, Elkon KB, Pusey CD, Hughes GR. Systemic Vasculitis with Asthma and Eosinophilia: A Clinical Approach to the Churg-Strauss Syndrome. Medicine (Baltimore). 1984;63(2):65-81. |
9 |
Reference no longer used |
10 |
Roufosse F, Kahn JE, Rothenberg ME, et al. Efficacy and Safety of Mepolizumab in Hypereosinophilic Syndrome: A Phase 3, Randomized, Placebo-Controlled Trial. J Allergy Clin Immunol. 2020. |
11 |
Valent P, Klion AD, Horny HP, et al. Contemporary Consensus Proposal on Criteria and Classification of Eosinophilic Disorders and Related Syndromes. J Allergy Clin Immunol. 2012;130(3):607-612. |
12 |
Shomali W, Gotlib J. World Health Organization-Defined Eosinophilic Disorders: 2019 Update on Diagnosis, Risk Stratification, and Management. Am J Hematol. 2019;94(10):1149-1167. |
13 |
Klion AD, Bochner BS, Gleich GJ, et al. Approaches to the Treatment of Hypereosinophilic Syndromes: A Workshop Summary Report. J Allergy Clin Immunol. 2006;117(6):1292-1302. |
14 |
Kuang FL, Klion AD. Biologic Agents for the Treatment of Hypereosinophilic Syndromes. J Allergy Clin Immunol Pract. 2017;5(6):1502-1509. |
15 |
Stevens WW, Schleimer RP, Kern RC. Chronic Rhinosinusitis with Nasal Polyps. J Allergy Clin Immunol Pract. 2016;4(4):565–572. |
16 |
Rank MA, Chu DK, Bognanni A, Oykhman P, Bernstein JA, Ellis AK, Golden DBK, Greenhawt M, Horner CC, Ledford DK, Lieberman J, Luong AU, Orlandi RR, Samant SA, Shaker MS, Soler ZM, Stevens WW, Stukus DR, Wang J, Peters AT. The Joint Task Force on Practice Parameters GRADE guidelines for the medical management of chronic rhinosinusitis with nasal polyposis. J Allergy Clin Immunol. 2023 Feb;151(2):386-398. doi: 10.1016/j.jaci.2022.10.026. Epub 2022 Nov 9. PMID: 36370881. |
17 |
Reference no longer used |
18 |
Orlandi, RR, Kingdom, TT, Smith, TL, et al. International consensus statement on rhinology and allergy: rhinosinusitis. Int Forum Allergy Rhinol. 2021; 11: 213– 739. https://doi.org/10.1002/alr.22741 |
19 |
National Asthma Education and Prevention Program Coordinating Committee Expert Panel Working Group. 2020 Focused updates to the asthma management guidelines. National Heart, Lung, and Blood Institute, 2007. Available at: https://www.nhlbi.nih.gov/health-topics/all-publications-and-resources/2020-focused-updates-asthma-management-guidelines |
20 |
Emmi, G., Bettiol, A., Gelain, E. et al. Evidence-Based Guideline for the diagnosis and management of eosinophilic granulomatosis with polyangiitis. Nat Rev Rheumatol 19, 378–393 (2023). https://doi.org/10.1038/s41584-023-00958-w |
POLICY AGENT SUMMARY PRIOR AUTHORIZATION
Target Brand Agent(s) |
Target Generic Agent(s) |
Strength |
Targeted MSC |
Available MSC |
Final Age Limit |
Preferred Status |
|
||||||
Fasenra pen |
benralizumab subcutaneous soln auto-injector |
30 MG/ML |
M ; N ; O ; Y |
N |
|
|
Nucala |
mepolizumab subcutaneous solution auto-injector |
100 MG/ML |
M ; N ; O ; Y |
N |
|
|
Nucala |
mepolizumab subcutaneous solution pref syringe |
100 MG/ML ; 40 MG/0.4ML |
M ; N ; O ; Y |
N |
|
|
POLICY AGENT SUMMARY QUANTITY LIMIT
Target Brand Agent Name(s) |
Target Generic Agent Name(s) |
Strength |
QL Amount |
Dose Form |
Day Supply |
Duration |
Addtl QL Info |
Allowed Exceptions |
Targeted NDCs When Exclusions Exist |
|
|||||||||
Fasenra pen |
Benralizumab Subcutaneous Soln Auto-injector 30 MG/ML |
30 MG/ML |
1 |
Pen |
56 |
DAYS |
*NOTE: Fasenra loading dose of 3 syringes for the first three months is approvable |
|
|
Nucala |
Mepolizumab Subcutaneous Solution Auto-injector 100 MG/ML |
100 MG/ML |
3 |
Syringes |
28 |
DAYS |
|
Severe eosinophilic asthma and CRSwNP: 1 syringe/28 days |
|
Nucala |
Mepolizumab Subcutaneous Solution Pref Syringe |
40 MG/0.4ML |
1 |
Syringe |
28 |
DAYS |
|
|
|
Nucala |
Mepolizumab Subcutaneous Solution Pref Syringe 100 MG/ML |
100 MG/ML |
3 |
Syringes |
28 |
DAYS |
|
Severe eosinophilic asthma and CRSwNP: 1 syringe/28 days |
|
ADDITIONAL QUANTITY LIMIT INFORMATION
Wildcard |
Target Brand Agent Name(s) |
Target Generic Agent Name(s) |
Strength |
Additional QL Information |
Targeted NDCs When Exclusions Exist |
Effective Date |
Term Date |
|
|||||||
4460402000D520 |
Fasenra pen |
Benralizumab Subcutaneous Soln Auto-injector 30 MG/ML |
30 MG/ML |
*NOTE: Fasenra loading dose of 3 syringes for the first three months is approvable |
|
|
|
CLIENT SUMMARY – PRIOR AUTHORIZATION
Target Brand Agent Name(s) |
Target Generic Agent Name(s) |
Strength |
Client Formulary |
Fasenra pen |
benralizumab subcutaneous soln auto-injector |
30 MG/ML |
Blue Partner ; Commercial ; GenPlus ; Health Insurance Marketplace ; NetResults A Series ; SourceRx |
Nucala |
mepolizumab subcutaneous solution auto-injector |
100 MG/ML |
Blue Partner ; Commercial ; GenPlus ; Health Insurance Marketplace ; NetResults A Series ; SourceRx |
Nucala |
mepolizumab subcutaneous solution pref syringe |
100 MG/ML ; 40 MG/0.4ML |
Blue Partner ; Commercial ; GenPlus ; Health Insurance Marketplace ; NetResults A Series ; SourceRx |
CLIENT SUMMARY – QUANTITY LIMITS
Target Brand Agent Name(s) |
Target Generic Agent Name(s) |
Strength |
Client Formulary |
Fasenra pen |
Benralizumab Subcutaneous Soln Auto-injector 30 MG/ML |
30 MG/ML |
Blue Partner ; Commercial ; GenPlus ; Health Insurance Marketplace ; NetResults A Series ; SourceRx |
Nucala |
Mepolizumab Subcutaneous Solution Auto-injector 100 MG/ML |
100 MG/ML |
Blue Partner ; Commercial ; GenPlus ; Health Insurance Marketplace ; NetResults A Series ; SourceRx |
Nucala |
Mepolizumab Subcutaneous Solution Pref Syringe |
40 MG/0.4ML |
Blue Partner ; Commercial ; GenPlus ; Health Insurance Marketplace ; NetResults A Series ; SourceRx |
Nucala |
Mepolizumab Subcutaneous Solution Pref Syringe 100 MG/ML |
100 MG/ML |
Blue Partner ; Commercial ; GenPlus ; Health Insurance Marketplace ; NetResults A Series ; SourceRx |
PRIOR AUTHORIZATION CLINICAL CRITERIA FOR APPROVAL
Module |
Clinical Criteria for Approval |
||
|
Initial Evaluation Target Agent(s) will be approved when ALL of the following are met:
Compendia Allowed: AHFS, DrugDex 1 or 2a level of evidence, or NCCN 1 or 2a recommended use Length of Approval: 6 months For Fasenra, approve loading dose for new starts and the maintenance dose for the remainder of the 6 months NOTE: If Quantity Limit applies, please refer to Quantity Limit Criteria
Renewal Evaluation Target Agent(s) will be approved when ALL of the following are met:
Compendia Allowed: AHFS, DrugDex 1 or 2a level of evidence, or NCCN 1 or 2a recommended use Length of Approval: 6 months NOTE: If Quantity Limit applies, please refer to Quantity Limit Criteria |
QUANTITY LIMIT CLINICAL CRITERIA FOR APPROVAL
Module |
Clinical Criteria for Approval |
|
Quantity Limit for the Target Agent(s) will be approved when ONE of the following is met:
Length of Approval: Initial: 6 months; For Fasenra, approve loading dose for new starts and the maintenance dose for the remainder of the 6 months; |
CONTRAINDICATION AGENTS
Contraindicated as Concomitant Therapy |
Agents NOT to be used Concomitantly Abrilada (adalimumab-afzb) Actemra (tocilizumab) Adalimumab Adbry (tralokinumab-ldrm) Amjevita (adalimumab-atto) Arcalyst (rilonacept) Avsola (infliximab-axxq) Benlysta (belimumab) Bimzelx (bimekizumab-bkzx) Cibinqo (abrocitinib) Cimzia (certolizumab) Cinqair (reslizumab) Cosentyx (secukinumab) Cyltezo (adalimumab-adbm) Dupixent (dupilumab) Enbrel (etanercept) Entyvio (vedolizumab) Fasenra (benralizumab) Hadlima (adalimumab-bwwd) Hulio (adalimumab-fkjp) Humira (adalimumab) Hyrimoz (adalimumab-adaz) Idacio (adalimumab-aacf) Ilaris (canakinumab) Ilumya (tildrakizumab-asmn) Inflectra (infliximab-dyyb) Infliximab Kevzara (sarilumab) Kineret (anakinra) Litfulo (ritlecitinib) Nucala (mepolizumab) Olumiant (baricitinib) Omvoh (mirikizumab-mrkz) Opzelura (ruxolitinib) Orencia (abatacept) Otezla (apremilast) Remicade (infliximab) Renflexis (infliximab-abda) Riabni (rituximab-arrx) Rinvoq (upadacitinib) Rituxan (rituximab) Rituxan Hycela (rituximab/hyaluronidase human) Ruxience (rituximab-pvvr) Siliq (brodalumab) Simponi (golimumab) Simponi ARIA (golimumab) Skyrizi (risankizumab-rzaa) Sotyktu (deucravacitinib) Stelara (ustekinumab) Taltz (ixekizumab) Tezspire (tezepelumab-ekko) Tremfya (guselkumab) Truxima (rituximab-abbs) Tysabri (natalizumab) Velsipity (etrasimod) Wezlana (ustekinumab-auub) Xeljanz (tofacitinib) Xeljanz XR (tofacitinib extended release) Xolair (omalizumab) Yuflyma (adalimumab-aaty) Yusimry (adalimumab-aqvh) Zeposia (ozanimod) Zymfentra (infliximab-dyyb) |
This pharmacy policy is not an authorization, certification, explanation of benefits or a contract. Eligibility and benefits are determined on a case-by-case basis according to the terms of the member’s plan in effect as of the date services are rendered. All pharmacy policies are based on (i) information in FDA approved package inserts (and black box warning, alerts, or other information disseminated by the FDA as applicable); (ii) research of current medical and pharmacy literature; and/or (iii) review of common medical practices in the treatment and diagnosis of disease as of the date hereof. Physicians and other providers are solely responsible for all aspects of medical care and treatment, including the type, quality, and levels of care and treatment.
The purpose of Blue Cross and Blue Shield of Alabama’s pharmacy policies are to provide a guide to coverage. Pharmacy policies are not intended to dictate to physicians how to practice medicine. Physicians should exercise their medical judgment in providing the care they feel is most appropriate for their patients.
Neither this policy, nor the successful adjudication of a pharmacy claim, is guarantee of payment.
ALBP _ Commercial _ CS _ Interleukin-5_(IL-5)_Inhibitors_PAQL _ProgSum_ 07-01-2024 _
© Copyright Prime Therapeutics LLC. May 2024 All Rights Reserved